1
40
30
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Text
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URL Address
<a href="http://doi.org/10.1172/jci119506" target="_blank" rel="noreferrer">http://doi.org/10.1172/jci119506</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Immune cell-derived beta-endorphin. Production, release, and control of inflammatory pain in rats
Publisher
An entity responsible for making the resource available
The Journal Of Clinical Investigation
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
Subject
The topic of the resource
Humans; Male; Time Factors; Analysis of Variance; Animals; Regression Analysis; Rats; Biomarkers of Pain; RNA; Genetic; Biomarkers Reference List; Inflammation/physiopathology; Freund's Adjuvant; Hindlimb; Pain/immunology/physiopathology; Corticotropin-Releasing Hormone/pharmacology; Wistar; Messenger/biosynthesis; beta-Endorphin/biosynthesis; Interleukin-1/pharmacology; Lymph Nodes/metabolism; Pro-Opiomelanocortin/biosynthesis; T-Lymphocytes/drug effects/immunology/metabolism; Transcription
Creator
An entity primarily responsible for making the resource
Cabot PJ; Carter L; Gaiddon C; Zhang Q; Schafer M; Loeffler JP; Stein C
Description
An account of the resource
Localized inflammation of a rat's hindpaw elicits an accumulation of beta-endorphin-(END) containing immune cells. We investigated the production, release, and antinociceptive effects of lymphocyte-derived END in relation to cell trafficking. In normal animals, END and proopiomelanocortin mRNA were less abundant in circulating lymphocytes than in those residing in lymph nodes (LN), suggesting that a finite cell population produces END and homes to LN. Inflammation increased proopiomelanocortin mRNA in cells from noninflamed and inflamed LN. However, END content was increased only in inflamed paw tissue and noninflamed LN-immune cells. Accordingly, corticotropin-releasing factor and IL-1beta released significantly more END from noninflamed than from inflamed LN-immune cells. This secretion was receptor specific, calcium dependent, and mimicked by potassium, consistent with vesicular release. Finally, both agents, injected into the inflamed paw, induced analgesia which was blocked by the co-administration of antiserum against END. Together, these findings suggest that END-producing lymphocytes home to inflamed tissue where they secrete END to reduce pain. Afterwards they migrate to the regional LN, depleted of the peptide. Consistent with this notion, immunofluorescence studies of cell suspensions revealed that END is contained predominantly within memory-type T cells. Thus, the immune system is important for the control of inflammatory pain. This has implications for the understanding of pain in immunosuppressed conditions like cancer or AIDS.
1997
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1172/jci119506" target="_blank" rel="noreferrer">10.1172/jci119506</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1997
Analysis of Variance
Animals
Backlog
beta-Endorphin/biosynthesis
Biomarkers of Pain
Biomarkers Reference List
Cabot PJ
Carter L
Corticotropin-Releasing Hormone/pharmacology
Freund's Adjuvant
Gaiddon C
Genetic
Hindlimb
Humans
Inflammation/physiopathology
Interleukin-1/pharmacology
Journal Article
Loeffler JP
Lymph Nodes/metabolism
Male
Messenger/biosynthesis
Pain/immunology/physiopathology
Pro-Opiomelanocortin/biosynthesis
Rats
Regression Analysis
RNA
Schafer M
Stein C
T-Lymphocytes/drug effects/immunology/metabolism
The Journal Of Clinical Investigation
Time Factors
transcription
Wistar
Zhang Q
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1152/jappl.2000.89.4.1561" target="_blank" rel="noreferrer">http://doi.org/10.1152/jappl.2000.89.4.1561</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Systemic hypoxia increases leukocyte emigration and vascular permeability in conscious rats.
Publisher
An entity responsible for making the resource available
Journal Of Applied Physiology (bethesda, Md. : 1985)
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
Subject
The topic of the resource
Male; Animals; Rats; Sprague-Dawley; Endothelium; Vascular/ph [Physiology]; Anoxia/pp [Physiopathology]; Capillary Permeability/ph [Physiology]; Endothelium; Leukocytes/ph [Physiology]; Venules/ph [Physiology]; Antioxidants/pd [Pharmacology]; Capillary Permeability/de [Drug Effects]; Catalase/pd [Pharmacology]; Cell Adhesion; Consciousness; Leukocytes/de [Drug Effects]; Nitric Oxide Donors/pd [Pharmacology]; Nitrogen Oxides; Reactive Oxygen Species/ph [Physiology]; Spermine/aa [Analogs & Derivatives]; Spermine/pd [Pharmacology]; Splanchnic Circulation/ph [Physiology]; Superoxide Dismutase/pd [Pharmacology]; Vascular/pp [Physiopathology]; Venules/pp [Physiopathology]
Creator
An entity primarily responsible for making the resource
Wood JG; Johnson JS; Mattioli LF; Gonzalez NC
Description
An account of the resource
We recently observed that acute systemic hypoxia produces rapid increases in leukocyte adherence in the mesenteric microcirculation of the anesthetized rat Wood JG, Johnson JS, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 1734-1740, 1999; Wood JG, Mattioli LF, and Gonzalez NC. J Appl Physiol 87: 873-881, 1999. Hypoxia-induced leukocyte adherence is associated with an increase in reactive oxygen species (ROS) generation and is attenuated by antioxidants or interventions that increase tissue levels of nitric oxide (NO). These results suggest that the acute effects of hypoxia on leukocyte-endothelial interactions are caused by a change in the ROS-NO balance. The present experiments were designed to extend our observations of the initial microcirculatory response to hypoxia; specifically, we wanted to determine whether the response to systemic hypoxia involves increased microvascular permeability and leukocyte emigration and whether ROS generation and decreased NO levels contribute to these responses. At this time, there is conflicting evidence, from in vitro studies, regarding the effect of hypoxia on these indexes of vascular function. Our studies were carried out in the physiological setting of the conscious animal, in which a prolonged hypoxic exposure is possible without the adverse effects that may develop under anesthesia. The central observation of these studies is that conscious animals exposed for 4 h to environmental hypoxia show increased microvascular permeability and emigration of leukocytes into the extravascular space of the mesenteric circulation. Furthermore, these events are dependent on increased ROS generation and, possibly, a subsequent decrease in tissue NO levels during systemic hypoxia. Our results show that systemic hypoxia profoundly affects vascular endothelial function through changes in the ROS-NO balance in the conscious animal.
2000
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jappl.2000.89.4.1561" target="_blank" rel="noreferrer">10.1152/jappl.2000.89.4.1561</a>
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Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2000
Animals
Anoxia/pp [Physiopathology]
Antioxidants/pd [Pharmacology]
Backlog
Capillary Permeability/de [Drug Effects]
Capillary Permeability/ph [Physiology]
Catalase/pd [Pharmacology]
Cell Adhesion
Consciousness
Endothelium
Gonzalez NC
Johnson JS
Journal Article
Journal Of Applied Physiology (bethesda, Md. : 1985)
Leukocytes/de [Drug Effects]
Leukocytes/ph [Physiology]
Male
Mattioli LF
Nitric Oxide Donors/pd [Pharmacology]
Nitrogen Oxides
Rats
Reactive Oxygen Species/ph [Physiology]
Spermine/aa [Analogs & Derivatives]
Spermine/pd [Pharmacology]
Splanchnic Circulation/ph [Physiology]
Sprague-Dawley
Superoxide Dismutase/pd [Pharmacology]
Vascular/ph [Physiology]
Vascular/pp [Physiopathology]
Venules/ph [Physiology]
Venules/pp [Physiopathology]
Wood JG
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
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URL Address
<a href="http://doi.org/10.1152/ajplung.1992.263.1.l88" target="_blank" rel="noreferrer">http://doi.org/10.1152/ajplung.1992.263.1.l88</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Chronic hypoxia selectively augments rat pulmonary artery Ca2+ and K+ channel-mediated relaxation.
Publisher
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The American Journal Of Physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1992
Subject
The topic of the resource
Male; Animals; Rats; Chronic disease; Inbred Strains; Anoxia/me [Metabolism]; Calcium Channels/ph [Physiology]; Potassium Channels/ph [Physiology]; Pulmonary Artery/me [Metabolism]; Vasoconstriction; Anoxia/pp [Physiopathology]; Calcium/me [Metabolism]; Cyclic AMP/ph [Physiology]; Cyclic GMP/ph [Physiology]; Endothelium; Extracellular Space/me [Metabolism]; Pulmonary Artery/de [Drug Effects]; Pulmonary Artery/pp [Physiopathology]; Vascular/ph [Physiology]; Vasodilator Agents/pd [Pharmacology]
Creator
An entity primarily responsible for making the resource
Rodman DM
Description
An account of the resource
The initiating event in hypoxic pulmonary hypertension is felt to be sustained hypoxic vasoconstriction, ultimately leading to vascular remodeling and fixed pulmonary hypertension. During the initial vasospastic phase endogenous vasodilatory pathways may serve to ameliorate the development of pulmonary hypertension. However, various studies in the systemic and pulmonary circulations have shown that chronic hemodynamic stress alters both endothelial and smooth muscle cell function. The effect of chronic hypoxia in rats was therefore tested on three major vasodilatory pathways: 1) endothelium-dependent relaxation (using endothelium-derived relaxing factor agonists and antagonists); 2) smooth muscle cell cyclic nucleotide-mediated relaxation [using guanosine and adenosine 3',5'-cyclic monophosphate (cGMP and cAMP) agonists]; and 3) ion channel-dependent relaxation (using K+ channel agonists and Ca2+ channel antagonists). It was found that short-term exposure (72 h) to hypoxia caused augmentation of K+ and Ca2+ channel-dependent relaxation with no effect on endothelium-dependent or cyclic nucleotide-mediated relaxation. More prolonged exposure (4-5 wk) was additionally associated with inhibition of endothelium-dependent relaxation and smooth muscle cell cGMP-mediated relaxation. There was no effect on either basal modulation of tone by the endothelium, cAMP-mediated relaxation, or systemic vessel relaxation. It is concluded that an early response to hemodynamic stress in the pulmonary circulation is alteration in smooth muscle cell ion channel function and/or Ca2+ homeostasis.
1992
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajplung.1992.263.1.l88" target="_blank" rel="noreferrer">10.1152/ajplung.1992.263.1.l88</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1992
Animals
Anoxia/me [Metabolism]
Anoxia/pp [Physiopathology]
Backlog
Calcium Channels/ph [Physiology]
Calcium/me [Metabolism]
Chronic Disease
Cyclic AMP/ph [Physiology]
Cyclic GMP/ph [Physiology]
Endothelium
Extracellular Space/me [Metabolism]
Inbred Strains
Journal Article
Male
Potassium Channels/ph [Physiology]
Pulmonary Artery/de [Drug Effects]
Pulmonary Artery/me [Metabolism]
Pulmonary Artery/pp [Physiopathology]
Rats
Rodman DM
The American Journal Of Physiology
Vascular/ph [Physiology]
Vasoconstriction
Vasodilator Agents/pd [Pharmacology]
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200108000-00036" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200108000-00036</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Opioid peptide-expressing leukocytes: identification, recruitment, and simultaneously increasing inhibition of inflammatory pain
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
Subject
The topic of the resource
Male; Pain Measurement; Analgesia; Animals; Rats; beta-Endorphin/blood; Biomarkers of Pain; Pain/physiopathology; Immunohistochemistry; Radioimmunoassay; Biomarkers Reference List; Wistar; Antibodies; Antigens; CD45/isolation & purification; Fluorescent Dyes; Hematopoietic Stem Cells/immunology; Immunomagnetic Separation; Inflammation/chemically induced/metabolism/pathology; Leukocytes/metabolism; Lymphocytes/immunology; Monoclonal/pharmacology; Opioid Peptides/biosynthesis
Creator
An entity primarily responsible for making the resource
Rittner HL; Brack A; Machelska H; Mousa SA; Bauer M; Schafer M; Stein C
Description
An account of the resource
BACKGROUND: Inflammatory pain can be effectively controlled by an interaction of opioid receptors on peripheral sensory nerve terminals with opioid peptides released from immune cells upon stressful stimulation. To define the source of opioid peptide production, we sought to identify and quantify populations of opioid-containing cells during the course of Freund's complete adjuvant-induced hind paw inflammation in the rat. In parallel, we examined the development of stress-induced local analgesia in the paw. METHODS: At 2, 6, and 96 h after Freund's complete adjuvant inoculation, cells were characterized by flow cytometry using a monoclonal pan-opioid antibody (3E7) and antibodies against cell surface antigens and by immunohistochemistry using a polyclonal antibody to beta-endorphin. After magnetic cell sorting, the beta-endorphin content was quantified by radioimmunoassay. Pain responses before and after cold water swim stress were evaluated by paw pressure thresholds. RESULTS: In early inflammation, 66% of opioid peptide-producing (3E7+) leukocytes were HIS48+ granulocytes. In contrast, at later stages (96 h), the majority of 3E7+ immune cells were ED1+ monocytes or macrophages (73%). During the 4 days after Freund's complete adjuvant inoculation, the number of 3E7+ cells increased 5.6-fold (P < 0.001, Kruskal-Wallis test) and the beta-endorphin content in the paw multiplied 3.9-fold (P < 0.05, Kruskal-Wallis test). In parallel, cold water swim stress-induced analgesia increased by 160% (P < 0.01, analysis of variance). CONCLUSIONS: The degree of endogenous pain inhibition is proportional to the number of opioid peptide-producing cells, and distinct leukocyte lineages contribute to this function at different stages of inflammation. These mechanisms may be important for understanding pain in immunosuppressed states such as cancer, diabetes, or AIDS and for the design of novel therapeutic strategies in inflammatory diseases.
2001
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200108000-00036" target="_blank" rel="noreferrer">10.1097/00000542-200108000-00036</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2001
Analgesia
Anesthesiology
Animals
Antibodies
Antigens
Backlog
Bauer M
beta-Endorphin/blood
Biomarkers of Pain
Biomarkers Reference List
Brack A
CD45/isolation & purification
Fluorescent Dyes
Hematopoietic Stem Cells/immunology
Immunohistochemistry
Immunomagnetic Separation
Inflammation/chemically induced/metabolism/pathology
Journal Article
Leukocytes/metabolism
Lymphocytes/immunology
Machelska H
Male
Monoclonal/pharmacology
Mousa SA
Opioid Peptides/biosynthesis
Pain Measurement
Pain/physiopathology
Radioimmunoassay
Rats
Rittner HL
Schafer M
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1073/pnas.91.10.4219" target="_blank" rel="noreferrer">http://doi.org/10.1073/pnas.91.10.4219</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Interleukin 1 beta and corticotropin-releasing factor inhibit pain by releasing opioids from immune cells in inflamed tissue
Publisher
An entity responsible for making the resource available
Proceedings Of The National Academy Of Sciences Of The United States Of America
Date
A point or period of time associated with an event in the lifecycle of the resource
1994
Subject
The topic of the resource
Humans; Male; Analysis of Variance; Animals; Regression Analysis; Rats; Biomarkers of Pain; Injections; Dose-Response Relationship; Drug; Naloxone/pharmacology; Enkephalin; Inflammation/immunology/physiopathology; Wistar; Antibodies/pharmacology; beta-Endorphin/immunology/physiology; Corticotropin-Releasing Hormone/administration & dosage/pharmacology/therapeutic use; Cyclosporine/pharmacology; Dynorphins/immunology/physiology; Endorphins/immunology/physiology/secretion; Interleukin-1/administration & dosage/pharmacology/therapeutic use; Leucine/analogs & derivatives/pharmacology; Methionine/immunology/physiology; Pain/immunology/physiopathology/prevention & control; Recombinant Proteins/pharmacology/therapeutic use; Somatostatin/analogs & derivatives/pharmacology
Creator
An entity primarily responsible for making the resource
Schafer M; Carter L; Stein C
Description
An account of the resource
Local analgesic effects of exogenous opioid agonists are particularly prominent in painful inflammatory conditions and are mediated by opioid receptors on peripheral sensory nerves. The endogenous ligands of these receptors, opioid peptides, have been demonstrated in resident immune cells within inflamed tissue of animals and humans. Here we examine in vivo and in vitro whether interleukin 1 beta (IL-1) or corticotropin-releasing factor (CRF) is capable of releasing these endogenous opioids and inhibiting pain. When injected into inflamed rat paws (but not intravenously), IL-1 and CRF produce antinociception, which is reversible by IL-1 receptor antagonist and alpha-helical CRF, respectively, and by the immunosuppressant cyclosporine A. In vivo administration of antibodies against opioid peptides indicates that the effects of IL-1 and CRF are mediated by beta-endorphin and, in addition, by dynorphin A and [Met]enkephalin, respectively. Correspondingly, IL-1 effects are inhibited by mu-, delta-, and kappa-opioid antagonists, whereas CRF effects are attenuated by all except a kappa-antagonist. Finally, IL-1 and CRF produce acute release of immunoreactive beta-endorphin in cell suspensions freshly prepared from inflamed lymph nodes. This effect is reversible by IL-1 receptor antagonist and alpha-helical CRF, respectively. These findings suggest that IL-1 and CRF activate their receptors on immune cells to release opioids that subsequently occupy multiple opioid receptors on sensory nerves and result in antinociception. beta-Endorphin, mu- and delta-opioid receptors play a major role, but IL-1 and CRF appear to differentially release additional opioid peptides.
1994
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1073/pnas.91.10.4219" target="_blank" rel="noreferrer">10.1073/pnas.91.10.4219</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1994
Analysis of Variance
Animals
Antibodies/pharmacology
Backlog
beta-Endorphin/immunology/physiology
Biomarkers of Pain
Carter L
Corticotropin-Releasing Hormone/administration & dosage/pharmacology/therapeutic use
Cyclosporine/pharmacology
Dose-Response Relationship
Drug
Dynorphins/immunology/physiology
Endorphins/immunology/physiology/secretion
Enkephalin
Humans
Inflammation/immunology/physiopathology
Injections
Interleukin-1/administration & dosage/pharmacology/therapeutic use
Journal Article
Leucine/analogs & derivatives/pharmacology
Male
Methionine/immunology/physiology
Naloxone/pharmacology
Pain/immunology/physiopathology/prevention & control
Proceedings Of The National Academy Of Sciences Of The United States Of America
Rats
Recombinant Proteins/pharmacology/therapeutic use
Regression Analysis
Schafer M
Somatostatin/analogs & derivatives/pharmacology
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1038/nm0897-831" target="_blank" rel="noreferrer">http://doi.org/10.1038/nm0897-831</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pain killers of the immune system
Publisher
An entity responsible for making the resource available
Nature Medicine
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
Subject
The topic of the resource
Animals; Rats; Biomarkers of Pain; RNA; Immunohistochemistry; Radioimmunoassay; beta-Endorphin/biosynthesis/physiology; Inflammation/pathology/physiopathology; Messenger/genetics; Pain/pathology/physiopathology; Pro-Opiomelanocortin/genetics; T-Lymphocytes/metabolism
Creator
An entity primarily responsible for making the resource
Sharp B; Yaksh T
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/nm0897-831" target="_blank" rel="noreferrer">10.1038/nm0897-831</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
Description
An account of the resource
1997
1997
Animals
Backlog
beta-Endorphin/biosynthesis/physiology
Biomarkers of Pain
Immunohistochemistry
Inflammation/pathology/physiopathology
Journal Article
Messenger/genetics
Nature Medicine
Pain/pathology/physiopathology
Pro-Opiomelanocortin/genetics
Radioimmunoassay
Rats
RNA
Sharp B
T-Lymphocytes/metabolism
Yaksh T
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0304-3959(01)00322-0" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0304-3959(01)00322-0</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Methionine-enkephalin-and Dynorphin A-release from immune cells and control of inflammatory pain
Publisher
An entity responsible for making the resource available
Pain
Date
A point or period of time associated with an event in the lifecycle of the resource
2001
Subject
The topic of the resource
Humans; Male; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Enkephalin; Biomarkers Reference List; Wistar; Antibodies/pharmacology; Corticotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/therapeutic use; Dynorphins/immunology/secretion; Inflammation/drug therapy/immunology/metabolism; Interleukin-2/pharmacology; Lymphocytes/drug effects/immunology/secretion; Methionine/immunology/metabolism; Pain/drug therapy/immunology/metabolism
Creator
An entity primarily responsible for making the resource
Cabot PJ; Carter L; Schafer M; Stein C
Description
An account of the resource
We have previously shown that beta-endorphin (END) is contained and released from memory-type T-cells within inflamed tissue and that it is capable to control pain (J Clin Invest 100(1) (1997) 142). Methionine-enkephalin (MET) and Dynorphin-A (DYN) are endogenous opioids with preference for delta- and kappa-opioid receptors, respectively. Both MET and DYN are produced and contained within immune cells. The goal of this study was to determine the release characteristics of MET and DYN in a rat model of localized hindpaw inflammation and to examine the antinociceptive role of MET and DYN in a Freund's adjuvant induced model of inflammatory pain. We found that corticotropin-releasing factor (CRF) can stimulate the release of both MET and DYN from lymphocytes. This release is dose-dependent and reversible by the selective CRF antagonist alpha-helical-CRF. Furthermore, CRF (1.5 ng) produces analgesia when injected into the inflamed paw, which is reversible by direct co-administration of antibodies to MET. Lymphocyte content of MET was 7.0+/-1.4 ng/million cells, whilst DYN content was ~30-fold lower. Both END and DYN, but not MET, were released by IL-1. Consistently, IL-1 produced peripheral analgesic effects which were not reversed by antibodies to MET. These results indicate that both MET and DYN play a role in peripheral analgesia but have different characteristics of release. These studies further support a role of the immune system in the control of inflammatory pain. This may be particularly important in patients suffering from compromised immune systems as with cancer and AIDS.
2001
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0304-3959(01)00322-0" target="_blank" rel="noreferrer">10.1016/s0304-3959(01)00322-0</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2001
Animals
Antibodies/pharmacology
Backlog
Biomarkers of Pain
Biomarkers Reference List
Cabot PJ
Carter L
Corticotropin-Releasing Hormone/antagonists & inhibitors/pharmacology/therapeutic use
Dose-Response Relationship
Drug
Dynorphins/immunology/secretion
Enkephalin
Humans
Inflammation/drug therapy/immunology/metabolism
Interleukin-2/pharmacology
Journal Article
Lymphocytes/drug effects/immunology/secretion
Male
Methionine/immunology/metabolism
Pain
Pain/drug therapy/immunology/metabolism
Rats
Schafer M
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0165-5728(99)00216-7" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0165-5728(99)00216-7</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Novel opioid peptides endomorphin-1 and endomorphin-2 are present in mammalian immune tissues
Publisher
An entity responsible for making the resource available
Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2000
Subject
The topic of the resource
Female; Humans; Male; Adult; Middle Aged; Animals; Rats; Non-U.S. Gov't; Research Support; Wistar; Radioimmunoassay/methods; Chromatography; High Pressure Liquid; Oligopeptides/analysis; Cross Reactions; Immune Sera/immunology; Immune System/chemistry; Spleen/chemistry; Thymus Gland/chemistry; Tissue Extracts/chemistry
Creator
An entity primarily responsible for making the resource
Jessop DS; Major GN; Coventry TL; Kaye SJ; Fulford AJ; Harbuz MS; De Bree FM
Description
An account of the resource
Endomorphin (EM)-1 and EM-2 are opioid tetrapeptides, reported within the central nervous system, which have very high specificity and affinity for the mu-opioid receptor. We have used newly developed and well-characterised radioimmunoassays (RIAs) in combination with reversed-phase high-performance liquid chromatography (HPLC) to detect EM-1 and EM-2 immunoreactivity (ir) in rat immune tissues. Endomorphins were detectable in extracts of rat spleen (total EM-1-ir/spleen: 440+/-73 pg, mean+/-SEM, a=group of eight rats; EM-2-ir: 150+/-12 pg) and thymus (EM-1-ir: 152+/-18 pg, mean+/-SEM n=8; EM-2-ir: 156+/-28 pg). EM-2-ir was detectable in extracts of human spleen (338+/-196 pg/g tissue, n=3). Multiple peaks of EM-1-ir and EM-2-ir were observed in rat spleen and thymus extracts, and multiple peaks of EM-2-ir were observed in extracts of human spleen, following reversed-phase HPLC and RIAs. This is the first report of endomorphin immunoreactivity in tissues of the rat and human immune systems.
2000
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0165-5728(99)00216-7" target="_blank" rel="noreferrer">10.1016/s0165-5728(99)00216-7</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2000
Adult
Animals
Backlog
Chromatography
Coventry TL
Cross Reactions
De Bree FM
Female
Fulford AJ
Harbuz MS
High Pressure Liquid
Humans
Immune Sera/immunology
Immune System/chemistry
Jessop DS
Journal Article
Journal Of Neuroimmunology
Kaye SJ
Major GN
Male
Middle Aged
Non-U.S. Gov't
Oligopeptides/analysis
Radioimmunoassay/methods
Rats
Research Support
Spleen/chemistry
Thymus Gland/chemistry
Tissue Extracts/chemistry
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/0928-4257(93)90034-q" target="_blank" rel="noreferrer">http://doi.org/10.1016/0928-4257(93)90034-q</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Brain and gut neuropeptides in peripheral blood mononuclear cells
Publisher
An entity responsible for making the resource available
Journal Of Physiology, Paris
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
Subject
The topic of the resource
Humans; Male; Adult; Aged; Middle Aged; Brain; Animals; Rats; 80 and over; Sprague-Dawley; Aging/metabolism; beta-Endorphin/blood/pharmacology; Chemotaxis/drug effects; Cholecystokinin/blood/pharmacology; Digestive System; Headache/blood; Lymphocytes/metabolism; Neuropeptides/blood; Schizophrenia/blood; Vasoactive Intestinal Peptide/blood/pharmacology
Creator
An entity primarily responsible for making the resource
Panerai AE; Sacerdote P
Description
An account of the resource
Neuropeptides, initially thought to be common features of gut and brain, are only synthesized in immune cells and modulate immune functions. The presence and possible functions of these peptides in immune cells in both physiological or pathological conditions have been investigated in our laboratory in the last years. Some of the data obtained are reviewed here, and future developments of the field are indicated.
1993
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0928-4257(93)90034-q" target="_blank" rel="noreferrer">10.1016/0928-4257(93)90034-q</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1993
80 And Over
Adult
Aged
Aging/metabolism
Animals
Backlog
beta-Endorphin/blood/pharmacology
Brain
Chemotaxis/drug effects
Cholecystokinin/blood/pharmacology
Digestive System
Headache/blood
Humans
Journal Article
Journal Of Physiology, Paris
Lymphocytes/metabolism
Male
Middle Aged
Neuropeptides/blood
Panerai AE
Rats
Sacerdote P
Schizophrenia/blood
Sprague-Dawley
Vasoactive Intestinal Peptide/blood/pharmacology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/0361-9230(93)90033-8" target="_blank" rel="noreferrer">http://doi.org/10.1016/0361-9230(93)90033-8</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Pituitary-adrenal function and hypothalamic beta-endorphin release in vitro following food deprivation
Publisher
An entity responsible for making the resource available
Brain Research Bulletin
Date
A point or period of time associated with an event in the lifecycle of the resource
1993
Subject
The topic of the resource
Male; Time Factors; Animals; Rats; Non-U.S. Gov't; Research Support; Body Weight; Blood Glucose/metabolism; Corticosterone/blood; In Vitro; Pituitary-Adrenal System/physiology; Adrenal Glands/physiology; beta-Endorphin/secretion; Corticotropin-Releasing Hormone/pharmacology; Dexamethasone/pharmacology; Food Deprivation; Hypothalamus/drug effects/secretion; Organ Size; Thymus Gland/physiology; Wistar
Creator
An entity primarily responsible for making the resource
Mitev Y; Almeida OF; Patchev V
Description
An account of the resource
Basal and dexamethasone-suppressed adrenal glucocorticoid secretion and hypothalamic beta-endorphin (BE) release in vitro were investigated in rats deprived of food for 24, 48, 72, and 96 h. Fasting for up to 48 h neither caused significant changes in serum corticosterone levels nor in the suppressive effect of dexamethasone. Food deprivation for 72-96 h resulted in increased basal serum corticosterone, diminished suppression by dexamethasone, and a significant involution of the thymus. Basal in vitro BE release from hypothalamic explants was significantly increased after the first day of food deprivation, and in vitro perifusion with corticotropin-releasing hormone (CRH) failed to enhance BE release further. With continuing food deprivation, basal BE release remained significantly greater than that from hypothalami originating from normally fed control rats. The stimulatory effect of CRH on BE release was only partially restored after 2 days of fasting. The results suggest that food deprivation for more than 2 days increases basal glucocorticoid secretion, and signs of impairment in hypothalamic-pituitary-adrenal regulation become apparent. These findings might be implicated in the pathogenetic mechanisms of endocrine dysregulation in diseases related to caloric reduction.
1993
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0361-9230(93)90033-8" target="_blank" rel="noreferrer">10.1016/0361-9230(93)90033-8</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1993
Adrenal Glands/physiology
Almeida OF
Animals
Backlog
beta-Endorphin/secretion
Blood Glucose/metabolism
Body Weight
Brain Research Bulletin
Corticosterone/blood
Corticotropin-Releasing Hormone/pharmacology
Dexamethasone/pharmacology
Food Deprivation
Hypothalamus/drug effects/secretion
In Vitro
Journal Article
Male
Mitev Y
Non-U.S. Gov't
Organ Size
Patchev V
Pituitary-Adrenal System/physiology
Rats
Research Support
Thymus Gland/physiology
Time Factors
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/0306-4522(92)90509-z" target="_blank" rel="noreferrer">http://doi.org/10.1016/0306-4522(92)90509-z</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Gene expression and localization of opioid peptides in immune cells of inflamed tissue: functional role in antinociception
Publisher
An entity responsible for making the resource available
Neuroscience
Date
A point or period of time associated with an event in the lifecycle of the resource
1992
Subject
The topic of the resource
Male; Pain Measurement; Analysis of Variance; Animals; Nucleic Acid Hybridization; Rats; Non-U.S. Gov't; Research Support; Biomarkers of Pain; RNA; Biomarkers Reference List; Inbred Strains; beta-Endorphin/genetics/metabolism; Calcitonin Gene-Related Peptide/analysis/metabolism; Endorphins/analysis/genetics/metabolism; Freund's Adjuvant; Gene Expression/radiation effects; Hindlimb; Inflammation/immunology/physiopathology; Messenger/genetics/metabolism; Nerve Fibers/physiology/ultrastructure; Oligonucleotide Probes; Pain/immunology/physiopathology; T-Lymphocytes/immunology/pathology; Whole-Body Irradiation
Creator
An entity primarily responsible for making the resource
Przewlocki R; Hassan AH; Lason W; Epplen C; Herz A; Stein C
Description
An account of the resource
Our previous studies indicate that endogenous opioids (primarily beta-endorphin) released during stressful stimuli can interact with peripheral opioid receptors to inhibit nociception in inflamed tissue of rats. This study sought to localize opioid precursor mRNAs and opioid peptides deriving therefrom in inflamed tissue, identify opioid containing cells and demonstrate their functional significance in the inhibition of nociception. In rats with Freund's adjuvant-induced unilateral hindpaw inflammation we show that: (i) pro-opiomelanocortin and proenkephalin-mRNAs (but not prodynorphin mRNA) are abundant in cells of inflamed, but absent in non-inflamed tissue; (ii) numerous cells infiltrating the inflamed subcutaneous tissue are stained intensely with beta-endorphin and [Met]enkephalin (but only few scattered cells with dynorphin) antibodies; (iii) beta-endorphin is present in T- and B-lymphocytes, monocytes and macrophages; and (iv) whole-body irradiation suppresses stress-induced antinociception in the inflamed paw. Taken together, these data suggest that endogenous opioid peptides are synthesized and processed within various types of immune cells at the site of inflammation. Immunosuppression abolishes the intrinsic antinociception in inflammatory tissue confirming the functional significance of these cells.
1992
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0306-4522(92)90509-z" target="_blank" rel="noreferrer">10.1016/0306-4522(92)90509-z</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1992
Analysis of Variance
Animals
Backlog
beta-Endorphin/genetics/metabolism
Biomarkers of Pain
Biomarkers Reference List
Calcitonin Gene-Related Peptide/analysis/metabolism
Endorphins/analysis/genetics/metabolism
Epplen C
Freund's Adjuvant
Gene Expression/radiation effects
Hassan AH
Herz A
Hindlimb
Inbred Strains
Inflammation/immunology/physiopathology
Journal Article
Lason W
Male
Messenger/genetics/metabolism
Nerve Fibers/physiology/ultrastructure
Neuroscience
Non-U.S. Gov't
Nucleic Acid Hybridization
Oligonucleotide Probes
Pain Measurement
Pain/immunology/physiopathology
Przewlocki R
Rats
Research Support
RNA
Stein C
T-Lymphocytes/immunology/pathology
Whole-Body Irradiation
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/0196-9781(91)90219-f" target="_blank" rel="noreferrer">http://doi.org/10.1016/0196-9781(91)90219-f</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Age-related changes of beta-endorphin and cholecystokinin in human and rat mononuclear cells
Publisher
An entity responsible for making the resource available
Peptides
Date
A point or period of time associated with an event in the lifecycle of the resource
1991
Subject
The topic of the resource
Humans; Male; Adult; Aged; Middle Aged; Animals; Rats; 80 and over; beta-Endorphin/blood; Lymphocyte Activation; Aging/blood/immunology; Cholecystokinin/blood; In Vitro; Interleukin-2/biosynthesis; Leukocytes; Mononuclear/immunology/metabolism
Creator
An entity primarily responsible for making the resource
Sacerdote P; Breda M; Barcellini W; Meroni PL; Panerai AE
Description
An account of the resource
Beta-endorphin (BE) and cholecystokinin (CCK) were measured in fresh PBMC isolated from human subjects and rats. The BE and CCK PBMC contents increased significantly with age both in human and rat models. Moreover, polyclonal stimulation induced a significant decrease of BE but not CCK contents in mononuclear cells from human aged subjects. The time course of changes in BE and CCK concentrations observed in fresh and cultured cells from subjects of different ages did not directly correlate to the time course of age-associated impairment of lectin-induced lymphocyte proliferative response and interleukin-2 synthesis. In fact, the lymphocyte functional defects were significantly observed only in the 71-99 year age group, whereas the neuropeptide changes were already evident in the 31-50 age group. Since BE has been shown to participate in the modulation of the immune system, the age-related modifications of PBMC BE could play a role in the immunodepression observed during aging.
1991
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0196-9781(91)90219-f" target="_blank" rel="noreferrer">10.1016/0196-9781(91)90219-f</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1991
80 And Over
Adult
Aged
Aging/blood/immunology
Animals
Backlog
Barcellini W
beta-Endorphin/blood
Breda M
Cholecystokinin/blood
Humans
In Vitro
Interleukin-2/biosynthesis
Journal Article
Leukocytes
Lymphocyte Activation
Male
Meroni PL
Middle Aged
Mononuclear/immunology/metabolism
Panerai AE
Peptides
Rats
Sacerdote P
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">http://doi.org/10.1006/brbi.1994.1023</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Intermittent but not continuous inescapable footshock stress affects immune responses and immunocyte beta-endorphin concentrations in the rat
Publisher
An entity responsible for making the resource available
Brain, Behavior, And Immunity
Date
A point or period of time associated with an event in the lifecycle of the resource
1994
Subject
The topic of the resource
Male; Time Factors; Animals; Acute Disease; Rats; Comparative Study; Receptors; beta-Endorphin/analysis; Corticosterone/blood; Corticotropin-Releasing Hormone/antagonists & inhibitors; Corticotropin-Releasing Hormone/blood/pharmacology/physiology; Electroshock/adverse effects; Foot; Helplessness; Killer Cells; Learned; Lymphocyte Activation; Lymphoid Tissue/chemistry; Natural/immunology; Neuroimmunomodulation/physiology; Peptide Fragments/pharmacology; Spleen/immunology; Sprague-Dawley; Stress/etiology/immunology
Creator
An entity primarily responsible for making the resource
Sacerdote P; Manfredi B; Bianchi M; Panerai AE
Description
An account of the resource
It is well known that a variety of stressors influence immune responses. The opioid peptide-beta-endorphin (BE) is deeply involved in stress responses, is synthesized in cells of the immune system, and participates in the modulation of immune function. We analyzed the ability of two different stress paradigms to modulate the beta-endorphin concentrations in the immune cells and the immune response in the rat. Two and 24 h after the exposure to inescapable intermittent footshock (1.6 mA, 60 Hz, 1 s, every 5 s for 20 min) the concentrations of beta-endorphin in splenocytes, peripheral blood mononuclear cells and lymph node cells were significantly increased. In contrast, the exposure to a continuous footshock for 3 min did not affect the concentrations of the opioid peptide. Similarly, phytohemoagglutinin-induced proliferation of splenocytes and natural killer activity were significantly impaired only after the exposure to intermittent footshock stress. On the contrary, plasma corticosterone levels were similarly elevated after both paradigms of stress. The pretreatment with the corticotropin-releasing hormone (CRH) receptor antagonist prevented both the stress-induced increase of immunocyte BE and immunosuppression. In conclusion, our data suggest that intermittent and continuous footshock stressors activate different neuroendocrine responses and that CRH plays a central role in mediating the immune effects of the intermittent footshock stress. The possible relationship between the beta-endorphin changes and immunosuppression is discussed.
1994
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1006/brbi.1994.1023" target="_blank" rel="noreferrer">10.1006/brbi.1994.1023</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1994
Acute Disease
Animals
Backlog
beta-Endorphin/analysis
Bianchi M
Brain, Behavior, And Immunity
Comparative Study
Corticosterone/blood
Corticotropin-Releasing Hormone/antagonists & inhibitors
Corticotropin-Releasing Hormone/blood/pharmacology/physiology
Electroshock/adverse effects
Foot
Helplessness
Journal Article
Killer Cells
Learned
Lymphocyte Activation
Lymphoid Tissue/chemistry
Male
Manfredi B
Natural/immunology
Neuroimmunomodulation/physiology
Panerai AE
Peptide Fragments/pharmacology
Rats
Receptors
Sacerdote P
Spleen/immunology
Sprague-Dawley
Stress/etiology/immunology
Time Factors
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1126/science.6254156" target="_blank" rel="noreferrer">http://doi.org/10.1126/science.6254156</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Fasting associated with decrease in hypothalamic beta-endorphin
Publisher
An entity responsible for making the resource available
Science
Date
A point or period of time associated with an event in the lifecycle of the resource
1980
Subject
The topic of the resource
Male; Time Factors; Animals; Rats; Non-U.S. Gov't; Research Support; Fasting; Corticotropin/metabolism; Endorphins/metabolism; Hypothalamus/metabolism; Pituitary Gland/metabolism
Creator
An entity primarily responsible for making the resource
Gambert SR; Garthwaite TL; Pontzer CH; Hagen TC
Description
An account of the resource
In rats that were fasted for 2 to 3 days there was a decline in hypothalamic, but not pituitary, beta-endorphin. There was no change in pituitary or hypothalamic adrenocorticotropin content as a result of fasting. Endogenous opiates may be involved in physiological adaptation to fasting.
1980
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1126/science.6254156" target="_blank" rel="noreferrer">10.1126/science.6254156</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1980
Animals
Backlog
Corticotropin/metabolism
Endorphins/metabolism
Fasting
Gambert SR
Garthwaite TL
Hagen TC
Hypothalamus/metabolism
Journal Article
Male
Non-U.S. Gov't
Pituitary Gland/metabolism
Pontzer CH
Rats
Research Support
Science
Time Factors
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1126/science.197601" target="_blank" rel="noreferrer">http://doi.org/10.1126/science.197601</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
beta-Endorphin and adrenocorticotropin are selected concomitantly by the pituitary gland
Publisher
An entity responsible for making the resource available
Science
Date
A point or period of time associated with an event in the lifecycle of the resource
1977
Subject
The topic of the resource
Male; Time Factors; Animals; Rats; Stress; Biomarkers of Pain; Amino Acid Sequence; Hypophysectomy; Corticotropin-Releasing Hormone/pharmacology; Adrenocorticotropic Hormone/blood/secretion; Endorphins/blood/secretion; Peptides/secretion; Physiological/blood; Pituitary Gland/secretion; Protein Precursors/secretion
Creator
An entity primarily responsible for making the resource
Guillemin R; Vargo T; Rossier J; Minick S; Ling N; Rivier C; Vale W; Bloom F
Description
An account of the resource
The opiate-like peptide beta-endorphin and adrenocorticotropin are concomitantly secreted in increased amounts by the adenohypophysis in response to acute stress or long-term adrenalectomy as well as in vitro in response to purified corticotropin releasing factor and other secretagogues. Conversely, administration of the synthetic glucocorticoid dexamethasone inhibits the secretion of both adrenocorticotropin and beta-endorphin. Thus, both hormones possess common and identical regulatory mechanisms and there may be a functional role for circulating beta-endorphin.
1977
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1126/science.197601" target="_blank" rel="noreferrer">10.1126/science.197601</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1977
Adrenocorticotropic Hormone/blood/secretion
Amino Acid Sequence
Animals
Backlog
Biomarkers of Pain
Bloom F
Corticotropin-Releasing Hormone/pharmacology
Endorphins/blood/secretion
Guillemin R
Hypophysectomy
Journal Article
Ling N
Male
Minick S
Peptides/secretion
Physiological/blood
Pituitary Gland/secretion
Protein Precursors/secretion
Rats
Rivier C
Rossier J
Science
Stress
Time Factors
Vale W
Vargo T
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/0304-3959(90)91112-v" target="_blank" rel="noreferrer">http://doi.org/10.1016/0304-3959(90)91112-v</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Peripheral opioid receptors mediating antinociception in inflammation. Activation by endogenous opioids and role of the pituitary-adrenal axis
Publisher
An entity responsible for making the resource available
Pain
Date
A point or period of time associated with an event in the lifecycle of the resource
1990
Subject
The topic of the resource
Male; Analysis of Variance; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Receptors; Naloxone/pharmacology; Foot; Biomarkers Reference List; Adrenalectomy; Cold; Endorphins/physiology; Hypophysectomy; Inbred Strains; Inflammation/physiopathology; Naltrexone/pharmacology; Nociceptors/physiopathology; Opioid/physiology; Pituitary-Adrenal System/physiology; Stress/physiopathology; Swimming
Creator
An entity primarily responsible for making the resource
Parsons CG; Czlonkowski A; Stein C; Herz A
Description
An account of the resource
This study investigated the involvement of endogenous opioid peptides in mediating cold water swim (CWS) stress-induced antinociception (SIA) in rats with unilateral hind paw inflammation induced by Freund's complete adjuvant (FCA). Following 0.5, 1 and 2 min of CWS, there was a duration-dependent elevation of paw pressure threshold (PPT) in both inflamed and non-inflamed paws which was maximal immediately after CWS and returned to control values within 15 min. The antinociception elicited in the inflamed paw was significantly greater than that elicited in the non-inflamed paw. The antinociception induced by a 1 min CWS was dose dependently antagonized by tertiary naloxone (0.125-1 mg/kg s.c.) and completely reversed by tertiary naltrexone (0.5 mg/kg). Quaternary naltrexone (5-40 mg/kg s.c.) was similarly effective in reversing the elevation of inflamed PPT induced by a 1 min CWS stress. In contrast, similar doses of quaternary naltrexone had no effect against centrally mediated morphine antinociception in non-inoculated rats. Adrenalectomy was without effect on the pattern of SIA seen in FCA-treated rats. Surgical hypophysectomy completely abolished the differential antinociception induced by 0.5 and 1 min durations of CWS but had little effect on that following 2 min of CWS stress. Inhibition of hypophysial corticotrophic cell secretion with dexamethasone (300 micrograms/kg) injected s.c. 120 min prior to CWS completely abolished the differential SIA at all durations of CWS tested. beta-Endorphin 12.5 micrograms/kg administered i.v. in non-stressed rats also caused a greater elevation of PPT in inflamed than in non-inflamed paws. This effect was not reversed by concomitant i.v. administration of (-) tertiary naloxone 5 mg/kg or quaternary naltrexone 20 mg/kg.
1990
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/0304-3959(90)91112-v" target="_blank" rel="noreferrer">10.1016/0304-3959(90)91112-v</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
1990
Adrenalectomy
Analysis of Variance
Animals
Backlog
Biomarkers of Pain
Biomarkers Reference List
Cold
Czlonkowski A
Dose-Response Relationship
Drug
Endorphins/physiology
Foot
Herz A
Hypophysectomy
Inbred Strains
Inflammation/physiopathology
Journal Article
Male
Naloxone/pharmacology
Naltrexone/pharmacology
Nociceptors/physiopathology
Opioid/physiology
Pain
Parsons CG
Pituitary-Adrenal System/physiology
Rats
Receptors
Stein C
Stress/physiopathology
Swimming
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1210/en.2003-1287" target="_blank" rel="noreferrer">http://doi.org/10.1210/en.2003-1287</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Subcellular pathways of beta-endorphin synthesis, processing, and release from immunocytes in inflammatory pain
Publisher
An entity responsible for making the resource available
Endocrinology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Animals; Rats; Biomarkers of Pain; Microscopy; Immunohistochemistry; Wistar; beta-Endorphin/biosynthesis; Carboxypeptidase H/metabolism; Extremities; Immunoelectron; Inflammation/immunology/metabolism; Leukocytes/drug effects/metabolism/ultrastructure; Norepinephrine/pharmacology; Pain/immunology/metabolism; Pro-Opiomelanocortin/metabolism; Proprotein Convertase 1/metabolism; Proprotein Convertase 2/metabolism; Secretory Vesicles/metabolism/ultrastructure; Sympathomimetics/pharmacology
Creator
An entity primarily responsible for making the resource
Mousa SA; Shakibaei M; Sitte N; Schafer M; Stein C
Description
An account of the resource
The opioid peptide beta-endorphin (END) as well as mRNA for its precursor proopiomelanocortin (POMC) are found not only in the pituitary gland, but also within various types of immune cells infiltrating inflamed sc tissue. During stressful stimuli END is released and interacts with peripheral opioid receptors to inhibit pain. However, the subcellular pathways of POMC processing and END release have not yet been delineated in inflammatory cells. The aim of the present study was to examine the presence of POMC, carboxypeptidase E, the prohormone convertases 1 (PC1), and 2 (PC2), PC2-binding protein 7B2, and the release of END from inflammatory cells in rats. Using immunohistochemistry we detected END and POMC alone or colocalized with PC1, PC2, carboxypeptidase E, and 7B2 in macrophages/monocytes, granulocytes, and lymphocytes of the blood and within inflamed sc paw tissue. Immunoelectron microscopy revealed that END is localized within secretory granules packed in membranous structures in macrophages, monocytes, granulocytes, and lymphocytes. Finally, END is released by noradrenaline from immune cells in vitro. Taken together, our results indicate that immune cells express the entire machinery required for POMC processing into functionally active peptides such as END and are able to release these peptides from secretory granules.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1210/en.2003-1287" target="_blank" rel="noreferrer">10.1210/en.2003-1287</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Animals
Backlog
beta-Endorphin/biosynthesis
Biomarkers of Pain
Carboxypeptidase H/metabolism
Endocrinology
Extremities
Immunoelectron
Immunohistochemistry
Inflammation/immunology/metabolism
Journal Article
Leukocytes/drug effects/metabolism/ultrastructure
Male
Microscopy
Mousa SA
Norepinephrine/pharmacology
Pain/immunology/metabolism
Pro-Opiomelanocortin/metabolism
Proprotein Convertase 1/metabolism
Proprotein Convertase 2/metabolism
Rats
Schafer M
Secretory Vesicles/metabolism/ultrastructure
Shakibaei M
Sitte N
Stein C
Sympathomimetics/pharmacology
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1152/jn.00353.2003" target="_blank" rel="noreferrer">http://doi.org/10.1152/jn.00353.2003</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Activation of peripheral NMDA receptors contributes to human pain and rat afferent discharges evoked by injection of glutamate into the masseter muscle
Publisher
An entity responsible for making the resource available
Journal Of Neurophysiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Female; Humans; Male; Adult; Analysis of Variance; Animals; Double-Blind Method; Cross-Over Studies; Rats; Non-U.S. Gov't; Research Support; Nonparametric; Statistics; Dose-Response Relationship; Drug; Receptors; Sprague-Dawley; Afferent Pathways/drug effects/physiology; Glutamic Acid/pharmacology; Masseter Muscle/drug effects/physiology; N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/metabolism; Pain/chemically induced/physiopathology
Creator
An entity primarily responsible for making the resource
Cairns BE; Svensson P; Wang K; Hupfeld S; Graven-Nielsen T; Sessle BJ; Berde CB; Arendt-Nielsen L
Description
An account of the resource
Peripheral N-methyl-d-aspartate (NMDA) receptors are found in deep tissues and may play a role in deep tissue pain. Injection of the endogenous NMDA receptor agonist glutamate into the masseter muscle excites deep craniofacial afferent fibers in rats and evokes pain in human subjects. It is not clear whether peripheral NMDA receptors play a role in these effects of glutamate. Accordingly, the effect of NMDA on afferent activity as well as the effect of locally administered NMDA receptor antagonists on glutamate-evoked afferent discharges in acutely anesthetized rats and muscle pain in human subjects was examined. Injection of NMDA into the masseter muscle evoked afferent discharges in a concentration-related manner. It was found that the NMDA receptor antagonists 2-amino-5-phosphonvalerate (APV, 10 mM), ketamine (10 mM), and dextromethorphan (40 mM) significantly decreased glutamate-evoked afferent discharges. The effects of APV and ketamine, but not dextromethorphan, were selective for glutamate-evoked afferent discharges and did not affect hypertonic saline-evoked afferent discharges. In human experiments, it was found that 10 mM ketamine decreased glutamate-evoked muscle pain but had no effect on hypertonic saline-evoked muscle pain. These results indicate that injection of glutamate into the masseter muscle evokes afferent discharges in rats and muscle pain in humans in part through activation of peripheral NMDA receptors. It is conceivable that activation of peripheral NMDA receptors may contribute to masticatory muscle pain and that peripherally acting NMDA receptor antagonists could prove to be effective analgesics for this type of pain.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/jn.00353.2003" target="_blank" rel="noreferrer">10.1152/jn.00353.2003</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2003
Adult
Afferent Pathways/drug effects/physiology
Analysis of Variance
Animals
Arendt-Nielsen L
Backlog
Berde CB
Cairns BE
Cross-Over Studies
Dose-Response Relationship
Double-Blind Method
Drug
Female
Glutamic Acid/pharmacology
Graven-Nielsen T
Humans
Hupfeld S
Journal Article
Journal Of Neurophysiology
Male
Masseter Muscle/drug effects/physiology
N-Methyl-D-Aspartate/agonists/antagonists & inhibitors/metabolism
Non-U.S. Gov't
Nonparametric
Pain/chemically induced/physiopathology
Rats
Receptors
Research Support
Sessle BJ
Sprague-Dawley
Statistics
Svensson P
Wang K
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1111/j.1749-6632.2002.tb04247.x" target="_blank" rel="noreferrer">http://doi.org/10.1111/j.1749-6632.2002.tb04247.x</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Opioid peptides endomorphin-1 and endomorphin-2 in the immune system in humans and in a rodent model of inflammation
Publisher
An entity responsible for making the resource available
Annals Of The New York Academy Of Sciences
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
Subject
The topic of the resource
Humans; Male; Animals; Rats; Non-U.S. Gov't; Research Support; Arthritis; Radioimmunoassay; Concanavalin A/pharmacology; Wistar; Spleen/chemistry; Thymus Gland/chemistry; Morphine/pharmacology; Apoptosis/drug effects; Experimental/immunology/metabolism; Lipopolysaccharides/pharmacology; Lymphocyte Activation/drug effects; Lymphocyte Subsets/chemistry/drug effects; Oligopeptides/analysis/pharmacology; Synovial Fluid/chemistry
Creator
An entity primarily responsible for making the resource
Jessop DS; Richards LJ; Harbuz MS
Description
An account of the resource
Endomorphin (EM)-1 and EM-2 are tetrapeptides with high affinity and selectivity for the micro-opioid receptor. We have utilized specific radioimmunoassays to characterize EM-1 and EM-2 in immune tissues from normal human subjects and from rats with adjuvant arthritis (AA). PBLs from three normal human subjects contained 248, 13, and 303 pg EM-1 per 100 million cells, whereas EM-2 was measured in two subjects at 69 and 588 pg per 100 million cells. In AA rats, EM-1 (but not EM-2) contents in the spleen and thymus were elevated compared with levels in tissues from non-AA controls. EM-1 was detectable in five of eight samples of synovial tissue from inflamed hind paws, whereas EM-2 was detectable in two of eight synovial extracts. Neither EM-1 nor EM-2 were detectable in synovial tissue from non-AA rats. To our knowledge, this is the first report of endomorphins in normal human immune cells. Increased endomorphin expression or uptake in peripheral tissues in a rodent model of chronic inflammation provides potential for endomorphins to selectively modulate chronic inflammation in mammals.
2002
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1111/j.1749-6632.2002.tb04247.x" target="_blank" rel="noreferrer">10.1111/j.1749-6632.2002.tb04247.x</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2002
Animals
Annals Of The New York Academy Of Sciences
Apoptosis/drug effects
Arthritis
Backlog
Concanavalin A/pharmacology
Experimental/immunology/metabolism
Harbuz MS
Humans
Jessop DS
Journal Article
Lipopolysaccharides/pharmacology
Lymphocyte Activation/drug effects
Lymphocyte Subsets/chemistry/drug effects
Male
Morphine/pharmacology
Non-U.S. Gov't
Oligopeptides/analysis/pharmacology
Radioimmunoassay
Rats
Research Support
Richards LJ
Spleen/chemistry
Synovial Fluid/chemistry
Thymus Gland/chemistry
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200407000-00031" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200407000-00031</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Tissue monocytes/macrophages in inflammation: hyperalgesia versus opioid-mediated peripheral antinociception
Publisher
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Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Analgesics; Animals; Rats; Biomarkers of Pain; Injections; Pain Measurement/drug effects; Freund's Adjuvant; Wistar; Flow Cytometry; Foot/pathology; Opioid/administration & dosage/pharmacology; Clodronic Acid/pharmacokinetics/pharmacology; Fentanyl/administration & dosage/pharmacology; Heat; Hyperalgesia/chemically induced/pathology/psychology; Inflammation/chemically induced/pathology; Liposomes; Macrophages/pathology; Monocytes/pathology; Non-Narcotic/pharmacokinetics/pharmacology; Pressure
Creator
An entity primarily responsible for making the resource
Brack A; Labuz D; Schiltz A; Rittner HL; Machelska H; Schafer M; Reszka R; Stein C
Description
An account of the resource
BACKGROUND: Opioid-containing leukocytes migrate to peripheral sites of inflammation. On exposure to stress, opioid peptides are released, bind to opioid receptors on peripheral sensory neurons, and induce endogenous antinociception. In later stages of Freund's complete adjuvant-induced local inflammation, monocytes/macrophages are a major opioid-containing leukocyte subpopulation, but these cells also produce proalgesic cytokines. In this study, the role of tissue monocytes/macrophages in hyperalgesia and in peripheral opioid-mediated antinociception was investigated. METHODS: After intraplantar injection of Freund's adjuvant, leukocyte subpopulations and opioid-containing leukocytes were analyzed by flow cytometry in the inflamed paw in the presence or absence of monocyte/macrophage depletion by intraplantar injection of clodronate-containing liposomes (phosphate-buffered saline and empty liposomes served as controls). Paw volume was measured with a plethysmometer. Hyperalgesia was determined by measuring heat-induced paw withdrawal latency and paw pressure threshold. Paw pressure threshold was also measured after swim stress and injection of fentanyl. RESULTS: At 48 and 96 h of inflammation, it was found that (1). monocytes/macrophages were the largest leukocyte subpopulation (> 55% of all leukocytes) and the predominant producers of opioid peptides (71-77% of all opioid-containing leukocytes in the paw), (2). clodronate-containing liposomes depleted monocytes/macrophages by 30-35% (P 0.05), and (4) opioid-containing leukocytes and swim stress but not fentanyl-induced antinociception were significantly decreased by clodronate-containing liposomes (P 0.05, all by t test; opioid-containing cells and swim stress-induced increase of paw pressure threshold were reduced by 35-42% and 20%, respectively). CONCLUSION: Partial depletion of tissue monocytes/macrophages impairs peripheral endogenous opioid-mediated antinociception without affecting hyperalgesia.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200407000-00031" target="_blank" rel="noreferrer">10.1097/00000542-200407000-00031</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Analgesics
Anesthesiology
Animals
Backlog
Biomarkers of Pain
Brack A
Clodronic Acid/pharmacokinetics/pharmacology
Fentanyl/administration & dosage/pharmacology
Flow Cytometry
Foot/pathology
Freund's Adjuvant
Heat
Hyperalgesia/chemically induced/pathology/psychology
Inflammation/chemically induced/pathology
Injections
Journal Article
Labuz D
Liposomes
Machelska H
Macrophages/pathology
Male
Monocytes/pathology
Non-Narcotic/pharmacokinetics/pharmacology
Opioid/administration & dosage/pharmacology
Pain Measurement/drug effects
Pressure
Rats
Reszka R
Rittner HL
Schafer M
Schiltz A
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200401000-00024" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200401000-00024</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Mobilization of opioid-containing polymorphonuclear cells by hematopoietic growth factors and influence on inflammatory pain
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Animals; Rats; Biomarkers of Pain; Inflammation/complications; RNA; Pain Measurement/drug effects; Radioimmunoassay; Pain/drug therapy/physiopathology; Wistar; Neutrophils/metabolism; Messenger/biosynthesis; DNA Primers; Reverse Transcriptase Polymerase Chain Reaction; Flow Cytometry; Cell Adhesion Molecules/pharmacology; Cell Separation; Chemokines/biosynthesis; Chemotaxis; Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology; Hindlimb/physiology; Leukocyte/drug effects; Light; Narcotics/metabolism/pharmacology; Stem Cell Factor/pharmacology
Creator
An entity primarily responsible for making the resource
Brack A; Rittner HL; Machelska H; Beschmann K; Sitte N; Schafer M; Stein C
Description
An account of the resource
BACKGROUND: Leukocytes can control inflammatory pain by secretion of opioid peptides, stimulated by cold-water swimming or local injection of corticotropin-releasing factor, and subsequent activation of opioid receptors on peripheral sensory neurons. This study investigated whether mobilization of polymorphonuclear cells (PMN) by granulocyte colony-stimulating factor (G-CSF) and stem cell factor (SCF) enhances immigration of opioid-containing PMN and peripheral opioid analgesia in rats with Freund complete adjuvant-induced hind paw inflammation. METHODS: In circulating PMN of rats treated with G-CSF+SCF and sham-treated rats, opioid peptide content was measured by radioimmunoassay. Expression of adhesion molecules (CD62L, CD49d, CD18), in vitro migration in the Boyden chamber, and infiltrating leukocytes were analyzed by flow cytometry. Chemokine messenger RNA transcription was quantified by LightCycler polymerase chain reaction. Paw pressure threshold was measured at baseline, after cold-water swimming, and after injection of corticotropin-releasing factor. RESULTS: G-CSF+SCF treatment increased circulating PMN (11-fold, P 0.05). CONCLUSIONS: G-CSF+SCF mobilized circulating opioid-containing PMN but had a minor influence on cell migration and peripheral analgesia, probably because of the low expression of chemokines in the inflamed paw and one of the decreased beta-endorphin content in PMN.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200401000-00024" target="_blank" rel="noreferrer">10.1097/00000542-200401000-00024</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Anesthesiology
Animals
Backlog
Beschmann K
Biomarkers of Pain
Brack A
Cell Adhesion Molecules/pharmacology
Cell Separation
Chemokines/biosynthesis
Chemotaxis
DNA Primers
Flow Cytometry
Granulocyte-Macrophage Colony-Stimulating Factor/pharmacology
Hindlimb/physiology
Inflammation/complications
Journal Article
Leukocyte/drug effects
Light
Machelska H
Male
Messenger/biosynthesis
Narcotics/metabolism/pharmacology
Neutrophils/metabolism
Pain Measurement/drug effects
Pain/drug therapy/physiopathology
Radioimmunoassay
Rats
Reverse Transcriptase Polymerase Chain Reaction
Rittner HL
RNA
Schafer M
Sitte N
Stein C
Stem Cell Factor/pharmacology
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1097/00000542-200301000-00030" target="_blank" rel="noreferrer">http://doi.org/10.1097/00000542-200301000-00030</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Modulation of peripheral endogenous opioid analgesia by central afferent blockade
Publisher
An entity responsible for making the resource available
Anesthesiology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Male; Analgesics; Animals; Rats; Injections; Immunohistochemistry; Spinal; Enkephalin; beta-Endorphin/metabolism; Wistar; Pain Threshold/drug effects; Neurons; Afferent/drug effects; Central Nervous System/drug effects; Endorphins/metabolism/physiology; Flow Cytometry; Foot/pathology; Inflammation/pathology; Methionine/metabolism; Morphine/administration & dosage/pharmacology; Opioid/administration & dosage/pharmacology; Peripheral Nerves/drug effects; Psychomotor Performance/drug effects
Creator
An entity primarily responsible for making the resource
Schmitt TK; Mousa SA; Brack A; Schmidt DK; Rittner HL; Welte M; Schafer M; Stein C
Description
An account of the resource
BACKGROUND: Peripheral tissue injury causes a migration of opioid peptide-containing immune cells to the inflamed site. The subsequent release and action of these peptides on opioid receptors localized on peripheral sensory nerve terminals causes endogenous analgesia. The spinal application of opioid drugs blocks the transmission of nociceptive information from peripheral injury. This study investigates the influence of exogenous spinal opioid analgesia on peripheral endogenous opioid analgesia. METHODS: Six and forty-eight hours after initiation of continuous intrathecal morphine infusion and administration of Freund's complete adjuvant into the hind paw of rats, antinociceptive and antiinflammatory effects were measured by paw pressure threshold, paw volume, and paw temperature, respectively. Inflammation and quantity of opioid-containing cells were evaluated by immunocytochemistry and flow cytometry. Cold water swim stress-induced endogenous analgesia was examined 24 h after discontinuation of intrathecal morphine administration. RESULTS: Intrathecal morphine (10 micro g/h) resulted in a significant and stable increase of paw pressure threshold ( P 0.05). At 48 but not at 6 h after Freund's complete adjuvant, the number of beta-endorphin-containing cells and cold water swim-induced antinociception were significantly reduced in intrathecal morphine-treated rats compared with those treated with intrathecal vehicle ( P< 0.05). CONCLUSIONS: These findings suggest an interplay of central and peripheral mechanisms of pain control. An effective central inhibition of pain apparently signals a reduced need for recruitment of opioid-containing immune cells to injured sites.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1097/00000542-200301000-00030" target="_blank" rel="noreferrer">10.1097/00000542-200301000-00030</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2003
Afferent/drug effects
Analgesics
Anesthesiology
Animals
Backlog
beta-Endorphin/metabolism
Brack A
Central Nervous System/drug effects
Endorphins/metabolism/physiology
Enkephalin
Flow Cytometry
Foot/pathology
Immunohistochemistry
Inflammation/pathology
Injections
Journal Article
Male
Methionine/metabolism
Morphine/administration & dosage/pharmacology
Mousa SA
Neurons
Opioid/administration & dosage/pharmacology
Pain Threshold/drug effects
Peripheral Nerves/drug effects
Psychomotor Performance/drug effects
Rats
Rittner HL
Schafer M
Schmidt DK
Schmitt TK
Spinal
Stein C
Welte M
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0165-5728(03)00213-3" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0165-5728(03)00213-3</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Different mechanisms of intrinsic pain inhibition in early and late inflammation
Publisher
An entity responsible for making the resource available
Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2003
Subject
The topic of the resource
Male; Time Factors; Pain Threshold; Animals; Rats; Biomarkers of Pain; Injections; Subcutaneous; Enkephalin; Hindlimb; Wistar; Corticotropin-Releasing Hormone/administration & dosage; Dynorphins/antagonists & inhibitors/biosynthesis/physiology; Edema/immunology/metabolism/physiopathology; Endorphins/antagonists & inhibitors/biosynthesis/physiology; Freund's Adjuvant/administration & dosage; Inflammation/immunology/metabolism/physiopathology; Leukocytes/drug effects/metabolism/physiology; Methionine/antagonists & inhibitors/biosynthesis/physiology; Naloxone/administration & dosage; Pain/immunology/pathology/prevention & control; Stress/immunology/metabolism/physiopathology
Creator
An entity primarily responsible for making the resource
Machelska H; Schopohl JK; Mousa SA; Labuz D; Schafer M; Stein C
Description
An account of the resource
Neuroimmune interactions control pain through activation of opioid receptors on sensory nerves by immune-derived opioid peptides. Here we evaluate mechanisms of intrinsic pain inhibition at different stages of Freund's adjuvant-induced inflammation of the rat paw. We use immunohistochemistry and paw pressure testing. Our data show that in early (6 h) inflammation leukocyte-derived beta-endorphin, met-enkephalin and dynorphin A activate peripheral mu-, delta- and kappa-receptors to inhibit nociception. In addition, central opioid mechanisms seem to contribute significantly to this effect. At later stages (4 days), antinociception is exclusively produced by leukocyte-derived beta-endorphin acting at peripheral mu and delta receptors. Corticotropin-releasing hormone (CRH) is an endogenous trigger of these effects at both stages. These findings indicate that peripheral opioid mechanisms of pain inhibition gain functional relevance with the chronicity of inflammation.
2003
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0165-5728(03)00213-3" target="_blank" rel="noreferrer">10.1016/s0165-5728(03)00213-3</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2003
Animals
Backlog
Biomarkers of Pain
Corticotropin-Releasing Hormone/administration & dosage
Dynorphins/antagonists & inhibitors/biosynthesis/physiology
Edema/immunology/metabolism/physiopathology
Endorphins/antagonists & inhibitors/biosynthesis/physiology
Enkephalin
Freund's Adjuvant/administration & dosage
Hindlimb
Inflammation/immunology/metabolism/physiopathology
Injections
Journal Article
Journal Of Neuroimmunology
Labuz D
Leukocytes/drug effects/metabolism/physiology
Machelska H
Male
Methionine/antagonists & inhibitors/biosynthesis/physiology
Mousa SA
Naloxone/administration & dosage
Pain Threshold
Pain/immunology/pathology/prevention & control
Rats
Schafer M
Schopohl JK
Stein C
Stress/immunology/metabolism/physiopathology
Subcutaneous
Time Factors
Wistar
-
Text
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Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/s0165-5728(02)00049-8" target="_blank" rel="noreferrer">http://doi.org/10.1016/s0165-5728(02)00049-8</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Immunohistochemical localization of endomorphin-1 and endomorphin-2 in immune cells and spinal cord in a model of inflammatory pain
Publisher
An entity responsible for making the resource available
Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2002
Subject
The topic of the resource
Male; Animals; Rats; Biomarkers of Pain; Immunohistochemistry; Freund's Adjuvant; Hindlimb; Wistar; Lymph Nodes/cytology; Lymphocytes/chemistry; Macrophages/chemistry; Monocytes/chemistry; Oligopeptides/analysis; Pain/chemically induced/immunology; Posterior Horn Cells/chemistry; Skin/chemistry/immunology/innervation
Creator
An entity primarily responsible for making the resource
Mousa SA; Machelska H; Schafer M; Stein C
Description
An account of the resource
Recently, two novel highly selective mu-opioid receptor (MOR) agonists, endomorphin-1 and endomorphin-2, have been isolated from bovine as well as human brains and were proposed to be the endogenous ligand for MOR. Later, endomorphin-1 and endomorphin-2 have been detected in the immune system of rats and humans using radioimmunoassay in combination with reverse-high-phase-liquid chromatography. In the present study, we analyzed the expression of endomorphin-1, endomorphin-2 and MOR by immunohistochemistry in a model of Freund's complete adjuvant (FCA)-induced painful inflammation. While MOR was upregulated on peripheral and central nerve terminals, inflammation did not alter endomorphin-2 expression in nerve fibers either in the dorsal horn of the spinal cord or in subcutaneous tissue. Endomorphin-1 and endomorphin-2 were expressed in immune cells (macrophage/monocytes) in the medullary region of the popliteal lymph nodes. The proportion of immunocytes (macrophage/monocytes, lymphocytes) containing endomorphin-1 and endomorphin-2 was increased in inflamed lymph nodes and subcutaneous paw tissue of animals with local inflammatory pain. Taken together, the upregulation of MOR and of its endogenous ligands endomorphin-1 and endomorphin-2 in immunocytes suggests an involvement of these opioid peptides in the peripheral control of inflammatory pain.
2002
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/s0165-5728(02)00049-8" target="_blank" rel="noreferrer">10.1016/s0165-5728(02)00049-8</a>
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Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2002
Animals
Backlog
Biomarkers of Pain
Freund's Adjuvant
Hindlimb
Immunohistochemistry
Journal Article
Journal Of Neuroimmunology
Lymph Nodes/cytology
Lymphocytes/chemistry
Machelska H
Macrophages/chemistry
Male
Monocytes/chemistry
Mousa SA
Oligopeptides/analysis
Pain/chemically induced/immunology
Posterior Horn Cells/chemistry
Rats
Schafer M
Skin/chemistry/immunology/innervation
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/j.pain.2004.08.029" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.pain.2004.08.029</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Control of inflammatory pain by chemokine-mediated recruitment of opioid-containing polymorphonuclear cells
Publisher
An entity responsible for making the resource available
Pain
Date
A point or period of time associated with an event in the lifecycle of the resource
2004
Subject
The topic of the resource
Male; Pain Measurement; Analysis of Variance; Animals; Rats; Non-U.S. Gov't; Research Support; Comparative Study; Dose-Response Relationship; Drug; Receptors; Naloxone/pharmacology; Freund's Adjuvant; Wistar; Flow Cytometry/methods; Antibodies/pharmacology; Cell Count/methods; Cell Movement/physiology; Chemokines; Chemokines/immunology/physiology; Corticotropin-Releasing Hormone/therapeutic use; CXC/immunology/metabolism; Drug Administration Routes; Enzyme-Linked Immunosorbent Assay/methods; Gene Expression Regulation/physiology; Immunohistochemistry/methods; Intercellular Signaling Peptides and Proteins/immunology/metabolism; Interleukin-8B/metabolism; Narcotics/metabolism; Neurogenic Inflammation/chemically induced/complications/therapy; Neutrophils/metabolism; Pain Threshold/drug effects; Pain/etiology/therapy
Creator
An entity primarily responsible for making the resource
Brack A; Rittner HL; Machelska H; Leder K; Mousa SA; Schafer M; Stein C
Description
An account of the resource
Opioid-containing leukocytes can counteract inflammatory hyperalgesia. Under stress or after local injection of corticotropin releasing factor (CRF), opioid peptides are released from leukocytes, bind to opioid receptors on peripheral sensory neurons and mediate antinociception. Since polymorphonuclear cells (PMN) are the predominant opioid-containing leukocyte subpopulation in early inflammation, we hypothesized that PMN and their recruitment by chemokines are important for peripheral opioid-mediated antinociception at this stage. Rats were intraplantarly injected with complete Freund's adjuvant (CFA). Using flow cytometry, immunohistochemistry, and ELISA, leukocyte subpopulations, chemokine receptor (CXCR2) expression on opioid-containing leukocytes and the CXCR2 ligands keratinocyte-derived chemokine (KC), macrophage inflammatory protein-2 (MIP-2) and cytokine-induced neutrophil chemoattractant-2 (CINC-2) were quantified. Paw pressure threshold (PPT) was determined before and after intraplantar and subcutaneous injection of CRF with or without naloxone. PMN depletion was achieved by intravenous injection of an antiserum. Chemokines were blocked by intraplantar injection of anti-MIP-2 and/or anti-KC antiserum. We found that at 2 h post CFA (i) intraplantar but not subcutaneous injection of CRF produced dose-dependent and naloxone-reversible antinociception (P0.05, ANOVA). In summary, in early inflammation peripheral opioid-mediated antinociception is critically dependent on PMN and their recruitment by CXCR2 chemokines.
2004
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.pain.2004.08.029" target="_blank" rel="noreferrer">10.1016/j.pain.2004.08.029</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2004
Analysis of Variance
Animals
Antibodies/pharmacology
Backlog
Brack A
Cell Count/methods
Cell Movement/physiology
Chemokines
Chemokines/immunology/physiology
Comparative Study
Corticotropin-Releasing Hormone/therapeutic use
CXC/immunology/metabolism
Dose-Response Relationship
Drug
Drug Administration Routes
Enzyme-Linked Immunosorbent Assay/methods
Flow Cytometry/methods
Freund's Adjuvant
Gene Expression Regulation/physiology
Immunohistochemistry/methods
Intercellular Signaling Peptides and Proteins/immunology/metabolism
Interleukin-8B/metabolism
Journal Article
Leder K
Machelska H
Male
Mousa SA
Naloxone/pharmacology
Narcotics/metabolism
Neurogenic Inflammation/chemically induced/complications/therapy
Neutrophils/metabolism
Non-U.S. Gov't
Pain
Pain Measurement
Pain Threshold/drug effects
Pain/etiology/therapy
Rats
Receptors
Research Support
Rittner HL
Schafer M
Stein C
Wistar
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1093/bja/aei287" target="_blank" rel="noreferrer">http://doi.org/10.1093/bja/aei287</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Opioids and the neuroimmune axis
Publisher
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British Journal Of Anaesthesia
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
Subject
The topic of the resource
Humans; Analgesics; Animals; Rats; Opioid; Receptors; Opioid Peptides/physiology; Opioid/pharmacology; Immune System/drug effects/physiology; Inflammation/immunology; mu/metabolism; Neuroimmunomodulation/immunology
Creator
An entity primarily responsible for making the resource
Williams JP; Lambert DG
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1093/bja/aei287" target="_blank" rel="noreferrer">10.1093/bja/aei287</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
Description
An account of the resource
2005
2005
Analgesics
Animals
Backlog
British Journal Of Anaesthesia
Humans
Immune System/drug effects/physiology
Inflammation/immunology
Journal Article
Lambert DG
mu/metabolism
Neuroimmunomodulation/immunology
Opioid
Opioid Peptides/physiology
Opioid/pharmacology
Rats
Receptors
Williams JP
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1073/pnas.0409888102" target="_blank" rel="noreferrer">http://doi.org/10.1073/pnas.0409888102</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
CB2 cannabinoid receptor activation produces antinociception by stimulating peripheral release of endogenous opioids
Publisher
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Proceedings Of The National Academy Of Sciences Of The United States Of America
Date
A point or period of time associated with an event in the lifecycle of the resource
2005
Subject
The topic of the resource
Humans; Male; Animals; Rats; Biomarkers of Pain; Cells; Cultured; Analgesics/pharmacology; Sprague-Dawley; beta-Endorphin/secretion; Cannabinoid; Cannabinoids; CB2/agonists/physiology; Endothelin B/physiology; Receptor
Creator
An entity primarily responsible for making the resource
Ibrahim MM; Porreca F; Lai J; Albrecht PJ; Rice FL; Khodorova A; Davar G; Makriyannis A; Vanderah TW; Mata HP; Malan TP
Description
An account of the resource
CB(2) cannabinoid receptor-selective agonists are promising candidates for the treatment of pain. CB(2) receptor activation inhibits acute, inflammatory, and neuropathic pain responses but does not cause central nervous system (CNS) effects, consistent with the lack of CB(2) receptors in the normal CNS. To date, there has been virtually no information regarding the mechanism of CB(2) receptor-mediated inhibition of pain responses. Here, we test the hypothesis that CB(2) receptor activation stimulates release from keratinocytes of the endogenous opioid beta-endorphin, which then acts at opioid receptors on primary afferent neurons to inhibit nociception. The antinociceptive effects of the CB(2) receptor-selective agonist AM1241 were prevented in rats when naloxone or antiserum to beta-endorphin was injected in the hindpaw where the noxious thermal stimulus was applied, suggesting that beta-endorphin is necessary for CB(2) receptor-mediated antinociception. Further, AM1241 did not inhibit nociception in mu-opioid receptor-deficient mice. Hindpaw injection of beta-endorphin was sufficient to produce antinociception. AM1241 stimulated beta-endorphin release from rat skin tissue and from cultured human keratinocytes. This stimulation was prevented by AM630, a CB(2) cannabinoid receptor-selective antagonist and was not observed in skin from CB(2) cannabinoid receptor-deficient mice. These data suggest that CB(2) receptor activation stimulates release from keratinocytes of beta-endorphin, which acts at local neuronal mu-opioid receptors to inhibit nociception. Supporting this possibility, CB(2) immunolabeling was detected on beta-endorphin-containing keratinocytes in stratum granulosum throughout the epidermis of the hindpaw. This mechanism allows for the local release of beta-endorphin, where CB(2) receptors are present, leading to anatomical specificity of opioid effects.
2005
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1073/pnas.0409888102" target="_blank" rel="noreferrer">10.1073/pnas.0409888102</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2005
Albrecht PJ
Analgesics/pharmacology
Animals
Backlog
beta-Endorphin/secretion
Biomarkers of Pain
Cannabinoid
Cannabinoids
CB2/agonists/physiology
Cells
Cultured
Davar G
Endothelin B/physiology
Humans
Ibrahim MM
Journal Article
Khodorova A
Lai J
Makriyannis A
Malan TP
Male
Mata HP
Porreca F
Proceedings Of The National Academy Of Sciences Of The United States Of America
Rats
Receptor
Rice FL
Sprague-Dawley
Vanderah TW
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/j.smrv.2005.08.001" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.smrv.2005.08.001</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Sleep deprivation and pain perception
Publisher
An entity responsible for making the resource available
Sleep Medicine Reviews
Date
A point or period of time associated with an event in the lifecycle of the resource
2006
Subject
The topic of the resource
Humans; Attitude; Animals; Rats; Sleep; Sprague-Dawley; Pain/epidemiology/physiopathology; REM/physiology; Sleep Deprivation/epidemiology/physiopathology
Creator
An entity primarily responsible for making the resource
Lautenbacher S; Kundermann B; Krieg JC
Description
An account of the resource
Chronically painful conditions are frequently associated with sleep disturbances, i.e. changes in sleep continuity and sleep architecture as well as increased sleepiness during daytime. A new hypothesis, which has attracted more and more attention, is that disturbances of sleep cause or modulate acute and chronic pain. Since it is well-known that pain disturbs sleep the relationship between the two has since recently been seen as reciprocal. To fathom the causal direction from sleep to pain we have reviewed experimental human and animal studies on the effects of sleep deprivation on pain processing. According to the majority of the studies, sleep deprivation produces hyperalgesic changes. Furthermore, sleep deprivation can interfere with analgesic treatments involving opioidergic and serotoninergic mechanisms of action. The still existing inconsistency of the human data and the exclusive focus on REM sleep deprivation in animals so far do not allow us to draw firm conclusions as to whether the hyperalgesic effects are due to the deprivation of specific sleep stages or whether they result from a generalized disruption of sleep continuity.
2006
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.smrv.2005.08.001" target="_blank" rel="noreferrer">10.1016/j.smrv.2005.08.001</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2006
Animals
Attitude
Backlog
Humans
Journal Article
Krieg JC
Kundermann B
Lautenbacher S
Pain/epidemiology/physiopathology
Rats
REM/physiology
Sleep
Sleep Deprivation/epidemiology/physiopathology
Sleep Medicine Reviews
Sprague-Dawley
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1038/sj.npp.1301393" target="_blank" rel="noreferrer">http://doi.org/10.1038/sj.npp.1301393</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Inhibition of inflammatory pain by CRF at peripheral, spinal and supraspinal sites: involvement of areas coexpressing CRF receptors and opioid peptides
Publisher
An entity responsible for making the resource available
Neuropsychopharmacology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
Subject
The topic of the resource
Male; Pain Measurement; Animals; Rats; Biomarkers of Pain; Dose-Response Relationship; Drug; Receptors; Freund's Adjuvant; Wistar; Animal; Disease Models; Analgesics/administration & dosage; Drug Administration Routes; Pain Threshold/drug effects; Brain/drug effects/metabolism; Spinal Cord/drug effects/metabolism; Corticotropin-Releasing Hormone/administration & dosage; Opioid Peptides/metabolism; Corticotropin-Releasing Hormone/metabolism; Ganglia; Hormone Antagonists/administration & dosage; Inflammation/chemically induced/complications; Pain/drug therapy/etiology/pathology; Sciatic Nerve/pathology; Spinal/drug effects/metabolism
Creator
An entity primarily responsible for making the resource
Mousa SA; Bopaiah CP; Richter JF; Yamdeu RS; Schafer M
Description
An account of the resource
There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist alpha-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissue--but not peripheral sensory neurons--that coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dose-dependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.
2007
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1038/sj.npp.1301393" target="_blank" rel="noreferrer">10.1038/sj.npp.1301393</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2007
Analgesics/administration & dosage
Animal
Animals
Backlog
Biomarkers of Pain
Bopaiah CP
Brain/drug effects/metabolism
Corticotropin-Releasing Hormone/administration & dosage
Corticotropin-Releasing Hormone/metabolism
Disease Models
Dose-Response Relationship
Drug
Drug Administration Routes
Freund's Adjuvant
Ganglia
Hormone Antagonists/administration & dosage
Inflammation/chemically induced/complications
Journal Article
Male
Mousa SA
Neuropsychopharmacology
Opioid Peptides/metabolism
Pain Measurement
Pain Threshold/drug effects
Pain/drug therapy/etiology/pathology
Rats
Receptors
Richter JF
Schafer M
Sciatic Nerve/pathology
Spinal Cord/drug effects/metabolism
Spinal/drug effects/metabolism
Wistar
Yamdeu RS
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
Citation List Month
Backlog
URL Address
<a href="http://doi.org/10.1016/j.jneuroim.2006.11.033" target="_blank" rel="noreferrer">http://doi.org/10.1016/j.jneuroim.2006.11.033</a>
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
A name given to the resource
Lymphocytes upregulate signal sequence-encoding proopiomelanocortin mRNA and beta-endorphin during painful inflammation in vivo
Publisher
An entity responsible for making the resource available
Journal Of Neuroimmunology
Date
A point or period of time associated with an event in the lifecycle of the resource
2007
Subject
The topic of the resource
Male; Time Factors; Animals; Rats; Biomarkers of Pain; RNA; beta-Endorphin/metabolism; Freund's Adjuvant; Wistar; Lymphocytes/metabolism; Flow Cytometry/methods; Gene Expression Regulation/drug effects/physiology; Inflammation/chemically induced/complications/pathology; Messenger/metabolism; Pain/etiology/pathology; Pro-Opiomelanocortin/genetics/metabolism; Protein Sorting Signals; Reverse Transcriptase Polymerase Chain Reaction/methods
Creator
An entity primarily responsible for making the resource
Sitte N; Busch M; Mousa SA; Labuz D; Rittner H; Gore C; Krause H; Stein C; Schafer M
Description
An account of the resource
Proopiomelanocortin (POMC)-derived beta-endorphin1-31 (END) released from immune cells inhibits inflammatory pain. We examined the expression of END and POMC mRNA encoding the signal sequence required for entry of the nascent polypeptide into the regulated secretory pathway in lymphocytes of rats with inflamed hindpaws. Within 12 h of inflammation, END increased in popliteal lymph nodes and at 96 h the intraplantar neutralization of END exacerbated pain. Lymphocytes expressed POMC, END, and full-length POMC mRNA. Semi-nested PCR revealed 8-fold increased exon 2-3 spanning POMC mRNA. Thus, painful inflammation enhances signal sequence-encoding lymphocytic POMC mRNA needed for regulated secretion of functionally active END.
2007
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1016/j.jneuroim.2006.11.033" target="_blank" rel="noreferrer">10.1016/j.jneuroim.2006.11.033</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. PedPalASCNET does not hold any rights over the resource listed here. All rights are retained by the journal listed under publisher and/or the creator(s).
Type
The nature or genre of the resource
Journal Article
2007
Animals
Backlog
beta-Endorphin/metabolism
Biomarkers of Pain
Busch M
Flow Cytometry/methods
Freund's Adjuvant
Gene Expression Regulation/drug effects/physiology
Gore C
Inflammation/chemically induced/complications/pathology
Journal Article
Journal Of Neuroimmunology
Krause H
Labuz D
Lymphocytes/metabolism
Male
Messenger/metabolism
Mousa SA
Pain/etiology/pathology
Pro-Opiomelanocortin/genetics/metabolism
Protein Sorting Signals
Rats
Reverse Transcriptase Polymerase Chain Reaction/methods
Rittner H
RNA
Schafer M
Sitte N
Stein C
Time Factors
Wistar